ORTHOPEDIC RHEUMATOLOGY

CHARACTERISTICS RHEUMATOID ARTHRITIS GOUTY ARTHRITIS OSTEOARTHRITIS

Pathology Chronic inflammatory disease (autoimmune) Metabolic disease Degenerative disease
↓ ↓ ↓
Body defense mechanism identifies normal Hyperuricemia Increased mechanical stress in some part
tissue as antigen and launch inflammatory rxn ↓ of articular cartilage
against it Impaired purine metabolism (d/t ↑ load or reduction of articular
↓ contact area – joint incongruity)
Crystal accumulation at the joint Articular cartilage functions to dissipate
forces. Loss of integrity → concentrated
forces in subchondral bone → focal
trabecular degeneration and cyst
formation and reactive sclerosis in zone
of maximal loading.
Cartilage at edges undergo growth and
endochondral ossification → osteophytes
Epidemiology Women > Men 3:1 Men > Women Men=Women (Increases with age)
Onset at any age Men: Middle age In women, more joints affected than men
Peaks at 35-50 years Women: Post-menopause
Speed of onset Insidious onset (Weeks to months) Hours → days Months
Causes Genetic predisposition (HLA-DRB-1) Primary gout (95%) Genetic predisposition (1st degree
+ Secondary gout relatives)
Environmental factor (viral infection, smoking) Prolonged hyperuricemia d/t Age, Increased mechanical stresses
- Acquired disorders Non modifiable
- Diuretics - Advancing age
- Renal failure - Female
- Tumor lysis syndrome Modifiable
Associated features - Obesity
Obesity - Previous injury
Hyperlipidemia - Malalignment
Hypertension - Work
Heavy alcohol use
Joint involvement Symmetrical, POLYARTICULAR Asymmetrical Asymmetrical
PIP, MCP, wrist Big toe (1st metatarsophalangeal joint), Weight bearing joints or joints with
forefoot, ankle, knee, wrist, elbow previous affliction
Knees, hips, vertebral column, fingers
Clinical features EARLY Acute gout Minimal signs of inflammation
(articular) Signs of inflammation Signs of inflammation Joint pain is worse after effort (evening
stiffness)
 - Polysynovitis with soft tissue swelling
and stiffness
- Joint pain is worse in morning (morning
stiffness) > 1 hour
LATE
Joint deformity more apparent
Joint instability + tendon rupture
↓ formation of tophi (chalky deposit of
Rheumatoid deformities
- Radial deviation of wrist
- Ulnar deviation of fingers
- Swan neck deformity (PIP ext, DIP flex)
- Boutonnierre deformity (PIP flex, DIP ext)
- Valgus knee, feet
Extraarticular Constitutional – muscle pain, LOW, fatigue,
manifestations general weakness
Monoarticular erythema, warmth
swelling over joint with extreme
tenderness. Skin – red, shiny, swollen
Fever may be present
Chronic gout
Marked by polyarticular arthritis and
MSU) - Subcutaneous, painless, firm,
nodular swellings
Site – digits of hands/feet, pinna, bursa
around elbow, knee, achilles tendon
More likely to occur in patients with
Polyarticular presentation, young onset
(<40yers)
Acute urate nephropathy
Precipitating factors (Dehydration/low
urine pH) → Urate crystals deposited
within renal tubules → obstruction and
ARF
Chronic urate nephropathy
Urate crystals deposited in interstitium
and renal medulla → inflammation and
surrounding fibrosis → chronic
irreversible renal failure
Urate nephrolithiasis
In gout 10X more than normal population
20% of gout p/w with stone
C/f – flank pain, ureteric colic, hematuria
- Joint pain (increased by joint use and
impact, relieved by rest). Night pain
might occur in severe OA
- Stiffness (occurs after inactivity ,
prolonged sitting– morning stiffness
only few minutes)
- +/- fullness and swelling of joint
- Gait disturbance → limp
- Bony swelling → decrease in function
- Loss of muscle bulk (inactivity)
- Limb deformity (enlargement of knee
joints → knock knees, bowing)
- Grinding sensation
- Instability
Signs
- Tenderness of soft tissues
- Joint swelling (mild synovitis)
- Crepitus
- Limited ROM
- Deformity
- Gait
Over a period of years, osteophytes and
soft tissue swelling produce a
characteristic knobbly appearance of DIP
joints (Herberden’s nodes)
PIP joint – Bouchard’s nodes
 - Rheumatoid nodules (granulomatous lesion Treat with urine alkalinization with
over bony points - olecranon) potassium citrate/sodium bicarbonate →
- Lympadenopathy dissolution of stone
- Vasculitis (leg ulcers)
- Serosal involvement (pleuritis, pericarditis)
- Ocular symptoms (keratoconjunctivitis,
scleritis)
- Neurological – cervical cord compression,
peripheral neuropathy
- Anemia
- Felty syndrome (RA + splenomegaly +
neutropenia)
- Sjogren syndrome (RA + dry eyes,mouth +
parotid enlargement)
Complications Fixed deformities, spinal cord compression, Joint deformity Baker’s cyst – OA of knee sometimes
systemic vasculitis, amyloidosis Urate nephropathy associated with marked effusion and
Urate nephrolithiasis herniation of posterior capsule
Fractures with tophaceous gout Spinal stenosis
Spondylolisthesis
Laboratory 1. FBC – Anemia, thrombocytosis Specific inv. to confirm gout Diagnosis of OA is mainly clinical. Blood
investigations 2. BUSE, LFT to determine suitable meds - Joint aspiration and crystal identification investigations and synovial fluid analysis
3. (+) Rheumatoid factor (RF) – autoAb - Serum urate (Upper limit is 420µmol/L) seldom required except to exclude other
4. (+) Anti CCP To detect presence of medical conditions diagnosis.
5. ↑ ESR, ↑ CRP associated with gout/hyperuricemia (-) RF
1. FBC Normal ESR, CRP
2. BUSE
3. Urinalysis
To detect complications
- Renal imaging
- Skeletal xrays
Radiological 1. Xray of joints 1. Xray of joints X-ray of affected joint should be done in
investigations Active – soft tissue swelling Acute – Soft tissue swelling weight bearing position for hip and knee.
Typical – Chronic tophaceous gout
- Joint space narrowing (joint destruction) Tophi – soft tissue abnormalities - Asymmetrical narrowing of joint space
- juxta articular bony erosion Erosive bony lesions - Punched out (progressive cartilage destruction)
- Osteoporosis Joint space normally preserved till severe - Subchondral sclerosis
2. Xray chest – pulmonary fibrosis disease - Subchondral cyst
3. Ultrasound of joint 2. Renal imaging (U/S) - Osteophytes
Erosion of joint, fluid accumulation
Diagnostic criteria Two of the following → clinical diagnosis Arthroscopy
1. Presence of clear hx of at least 2 May show cartilage damage before xray
attacks of painful joint swelling changes appear.
2. A clear hx or observation of
podagra
3. Presence of tophus
4. Rapid response to colchicine
within 48 hours of starting
treatment
Definitive diagnosis
- Crystals of MSU seen in synovial
fluid or in the tissues

Treatment Main aim 1. Lifestyle modification and dietary Aim

1. Control pain advice
NSAIDs - Maintain/achieve healthy body weight
Intraarticular long acting corticosteroids - Restriction/elimination of alcohol
2. Prevent deformity - Adequate fluid intake 2-3L/day
3. Keep disease under control - Restrict consumption of purine rich
food (red meat, seafood)
Diagnosis → Start treatment within 3 months - Control of comorbidities (HPL,HTN)
(X delay to present erosion)
2. Acute gouty arthritis
Start with prednisolone + methotrexate Aim- reduce pain and inflammation
(bridging therapy) 1st line – Rest + NSAIDS/Cox-2 inhibitors
↓ 3 months later 2nd line
Remission? - Colchicine (S/E – abdominal pain,
- Use DAS 28 to monitor disease activity diarrhea, N/V)
- Optimize by increasing dose/changing - Intraarticular injection of
drug/ combination glucocorticoid (In elderly/those
with renal insufficiency, hepatic
DMARD dysfunction, cardiac failure, PUD)
1. Methotrexate (Start at 7.5mg/week)
Takes 2.5 months to work 3. Chronic gouty arthritis
S/E – hepatitis, bone marrow suppression Aim
2. Sulfasalazine - Lower serum urate levels in those
3. Leflunomide with recurrent attacks of GA,
4. Hydrochloroquine erosive GA, tophi)
1. Maintain movement and muscle
strength
2. Protect joint from overload
3. Relieve pain
4. Modify daily activities
Physical therapy – Mainstay of treatment
in early case
Aerobic exercise to maintain joint
mobility and improve muscle strength
Load reduction – Weight reduction, shock
absorbing shoes, avoid activities like
climbing stairs, using walking stick
Analgesic
Intermediate treatment
- Joint debridement (removal of loose
bodies, cartilage tags, interfering
osteophytes) via arthroscopy or
open.
 Good in combination. Alone is weak
inflammatory suppressor
If severe at presentation, start with
combination therapy + prednisolone and
consider biologic tx
Biologic therapy
- TNF inhibitor (very very very expensive)
Surgery
Early
- Soft tissue procedures (synovectomy,
tendon repair/replacement, joint
stabilization)
Late
- Reconstructive surgery
Indication – severe joint destruction, fixed
deformity, loss of function
Options – arthrodesis, osteotomy, arthroplasty
- Lower serum urate to - Corrective osteotomy. In case of
<360µmol/L localized articular overload from joint
Hypouricemic therapy –Should only be malalignment
started after acute attack well controlled
(2 weeks) Late treatment
Or else may prolong attack or lead to Reconstructive surgery
rebound flares. For the same reason, For progressive joint destruction with
should not be stopped or adjusted during increasing pain, instability and deformity
acute attack
- Realignment osteotomy
- Allopurinol (xanthine oxidase - Arthroplasty
inhibitor - ↓ conversion to uric - Arthrodesis
acid
- Probenicid (uricosuric-need high
urine excretion otherwise stone
formation). Contraindicated in
renal impairment
Radiological Active – soft tissue swelling
investigations Typical –
- Joint space narrowing (joint destruction)
- juxta articular bony erosion
- Osteoporosis
Acute – Soft tissue swelling
Chronic tophaceous gout
Tophi – soft tissue abnormalities
Erosive bony lesions - Punched out
Joint space normally preserved till severe
disease
X-ray of affected joint should be done in
weight bearing position for hip and knee.
- Asymmetrical narrowing of joint space
(progressive cartilage destruction)
- Subchondral sclerosis
- Subchondral cyst
- Osteophytes